Biomedical subjects

A Rumley

Publications and source records attributed to A Rumley.

At least 91 records · Page 5Linked to original sources

PubMed1996

Clinical, biochemical, and rheologic factors affecting the outcome of infrainguinal bypass grafting.

PURPOSE: The purpose of this study was to determine the effects of patient characteristics, blood rheology, and plasma biochemistry on the outcome of infrainguinal bypass grafting. METHODS: Blood rheology, plasma fibrinogen, cross-linked fibrin degradation products, von Willebrand factor (vWf) and other endothelial products, and clinical variables including smoking markers were determined before surgery in patients with 184 consecutive infrainguinal bypass grafts (90 vein, 94 synthetic grafts). RESULTS: Fifty (27%) graft occlusions and 17 (9%) deaths occurred within 1 year of surgery. On univariate analysis a poor outcome was associated with elevated preoperative plasma fibrinogen, fibrin degradation products, vWf, and platelet levels, reduced hemoglobin and systolic ankle pressure, a below-knee anastomosis, a decrease in patent calf vessels, and the presence of tissue necrosis (all p < 0.001). On multivariate analysis increased preoperative vWf levels were predictive of poor postoperative outcome (relative hazard for upper quartile versus lower quartile = 1.82), as were a low systolic ankle pressure (relative hazard = 2.51), presence of tissue necrosis (relative hazard = 2.73), and female sex (relative hazard = 1.9). None of the other variables studied was related to outcome. With a preoperative risk score derived from the results, graft patency rates within 3 months of surgery fell to less than 25% with risk scores in the upper quartile. CONCLUSIONS: Preoperative measurement of plasma vWf may enable more accurate prediction of the outcome of infrainguinal revascularization and when combined with other variables could assist in patient selection for these procedures. The association of vWf with graft occlusion supports a role for endothelial disturbance in graft occlusion.

Adult↗

PubMed1996

Variation in cardiovascular risk factors by angiographic site of lower limb atherosclerosis.

OBJECTIVE: To determine differences in the levels of the cardiovascular risk factors, cigarette smoking, serum lipids and blood pressure, between three groups of patients with different sites of lower limb atherosclerosis. DESIGN: Cross-sectional survey of a consecutive series of patients with symptoms of either intermittent claudication or rest pain. METHODS AND MATERIALS: One hundred and ninety-two men and women who had undergone angiography were classified using the Bollinger scoring system into groups with predominantly aortoiliac, femoropopliteal or dual-site disease. History of cigarette smoking, serum cotinine, serum thiocyanate, total cholesterol and HDL cholesterol were estimated. Systolic and diastolic pressures were measured and the ankle brachial pressure index (ABPI) was calculated. RESULTS: Eighty-five patients were classified as having femoropopliteal disease, 34 aortoiliac disease and 73 dual-site disease. After adjusting for age, sex and severity of disease, aortoiliac patients were significantly younger (p </- 0.001), more likely to be female and current smokers, and had the highest levels of diastolic blood pressure. Life time cigarette consumption (pack-years) and total cholesterol concentrations were highest in femoropopliteal disease. Patients with dual-site disease were more likely to have had a myocardial infarction and angina pectoris (p </- 0.05). Systolic blood pressure was also highest in this group. CONCLUSION: different levels of cardiovascular risk factors may predispose individuals to atherosclerosis at different sites in the lower limb. Large population studies would be required to delineate the risks more precisely.

Adult↗

PubMed1996

Haemostatic and rheological factors in intermittent claudication: the influence of smoking and extent of arterial disease.

Patients with intermittent claudication have been reported to have disturbances in blood rheology and haemostasis. Whether these disturbances are a result of, or largely independent of, smoking history and arterial narrowing has not yet been established. The levels of whole blood and plasma viscosity, haematocrit, von Willebrand factor antigen, fibrin D-dimer antigen and urinary fibrinopeptide A antigen were compared in 617 claudicants and 722 controls from two epidemiological studies in Edinburgh. After adjustment for age and sex, all factors, except whole blood viscosity and haematocrit, were significantly higher in the claudicants compared to controls (P < or = 0.001). The risk of intermittent claudication was significantly raised for unit change in each factor, except for whole blood viscosity and haematocrit. Adjustment for lifetime smoking had little effect on the odds ratios. After further adjustment for the ankle brachial pressure index (as a measure of the extent of peripheral arterial disease), haematocrit, von Willebrand factor and urinary fibrinopeptide A showed a significant independent relationship with the risk of intermittent claudication. We conclude that the association between selected rheological and haemostatic factors and leg ischaemia is largely independent of both smoking history and the extent of arterial narrowing, and may be directly related to microvascular ischaemia.

Aged↗

PubMed1996

Haemostatic factors, atherosclerosis and risk of abdominal aortic aneurysm.

Abdominal aortic aneurysms have traditionally been thought to be a consequence of severe atherosclerosis of the arterial wall. To date, the role of haemostatic factors in aneurysmal disease has not been extensively researched. The aim of this study was to see if such factors were independently related to the occurrence of aortic aneurysm. Furthermore, were the associations maintained after taking into account the presence of underlying atherosclerotic disease? Using data from the Edinburgh Artery Study, a nested case-control design was used involving 40 cases of aortic aneurysm, each being matched to five controls by sex and within a 5-year age band. After adjustment for age and sex, both fibrinogen (P < or = 0.01) and fibrin D-dimer (P < or = 0.001) were each associated with a significant increased risk of aneurysm. Further adjustment for packyears, history of cardiovascular disease and the ankle brachial pressure index resulted in odds ratios of 1.51 (95% CI 1.05 to 2.16, P < or = 0.05) for fibrinogen and 3.75 (95% CI 1.80 to 7.82, P < or = 0.001) for fibrin D-dimer. These associations probably arise as a consequence of fibrin deposition and turnover within the aneurysmal sac, although further prospective studies are needed before thrombotic factors can be used in the identification of a group who are at high risk of developing an abdominal aortic aneurysm.

Aged↗

PubMed1996

Blood viscosity, coagulation, and activated protein C resistance in central retinal vein occlusion: a population controlled study.

BACKGROUND: The role of blood viscosity and haemostasis has been investigated in mixed groups of patients with branch and central retinal vein occlusion (CRVO) with conflicting results. This may have partly been due to the different aetiologies of these two types of vein occlusion. METHODS: In this study viscosity and coagulation (including activated protein C resistance) were examined in 87 patients with CRVO and compared with the results from an age-matched, population based control group. RESULTS: Viscosity variables were higher in CRVO than in controls which suggested that reduced red cell deformability was associated with the occurrence of CRVO. A higher percentage of the patients with CRVO (12%) had activated protein C resistance than controls (5%). Patients who developed the complication of iris neovascularisation had relatively low antithrombin III, factor VII, and tissue plasminogen activator indicating both a tendency to thrombus formation and a reduction in fibrinolytic activity. CONCLUSION: Increased blood viscosity may contribute to the production of CRVO by inducing stasis of blood flow, with thrombus formation in at risk individuals who go on to develop iris neovascularisation.

Adult↗

PubMed1996

Thrombogenesis in mitral regurgitation and aortic stenosis.

The exact mechanisms for thrombus formation in patients with valvular heart disease have not been clearly defined. Abnormalities in plasma coagulation factors indicative of a prothrombotic state may in part account for the risk of stroke and thromboembolism in such patients. The aim of this study was, therefore, to determine the effects of mitral regurgitation (MR) and aortic stenosis (AS) on plasma fibrinogen or fibrin D-dimer levels as indices of a thrombogenic (or prothrombotic) state. A total of 25 patients with valve disease in sinus rhythm were studied: 12 patients (all women; mean age fifty-five years, sem 3.3) with MR; and 13 patients (7 men, 6 women; mean age fifty-seven years, sem 3.5) with AS were studied. Patients with MR had a median plasma fibrinogen that was significantly elevated when compared with female population values (median difference 0.62 g/L; 95% confidence intervals (CI) 0.27 to 1.05, P = 0.0016). However, these patients had a median plasma fibrin D-dimer that was lower than that for population controls (median difference 21 ng/mL; 95% CI 0 to 38, P = 0.05). Patients with aortic valve disease had a median plasma fibrinogen that was significantly increased when compared with population controls (median difference 0.82 g/L; 95% CI 0.34 to 1.24, P = 0.001). These patients had a plasma fibrin D-dimer level that was similar to population values (median difference 3 ng/mL; 95% CI -25 to 22, P = 0.80). Patients with MR or AS have higher plasma fibrinogen levels when compared with "normal" population values, suggesting possible hemorheologic abnormalities in these patients. Subjects with MR had lower plasma fibrin D-dimer levels, suggesting lesser intravascular clotting, consistent with clinical echocardiographic studies. Subjects with AS had plasma fibrin D-dimer levels similar to the "normal" population values, suggestive of a different pathophysiological mechanism for thromboembolism. These findings add to an improved understanding of the relationship between clinical observations and the significance of plasma fibrinogen and fibrin D-dimer levels in thrombogenesis.

Aortic Valve Stenosis↗

PubMed1996

Smoking, haemostatic factors and the severity of aorto-iliac and femoro-popliteal disease.

To determine relationships between haemostatic and rheological factors and severity of peripheral atherosclerosis and differences by site, an angiographic cross-sectional survey was carried out on 192 men and women with intermittent claudication or rest pain. 34 patients were classified as having aorto-iliac disease, 85 femoro-popliteal disease and 73 dual-site disease. Mean levels of haemostatic or rheological factors did not differ significantly between the three site groups. In all 192 patients, disease severity in the femoro-popliteal segments was correlated with plasma nephelometric fibrinogen (r = 0.20, p < or = 0.01), von Willebrand factor (r = 0.14, p < or = 0.05) and fibrin D-dimer (r = 0.22, p < or = 0.001). On multiple regression analyses, fibrinogen was independently associated with disease severity in the femoro-popliteal segments (p < or = 0.05), but not in the aorto-iliac segments. Adjustment for packyears or serum thiocyanate had little effect on the association of fibrinogen with severity of disease. An inverse relationship between plasminogen activator inhibitor and disease severity in the femoro-popliteal segments was found only in men (r = 0.24, p < or = 0.01). We conclude that elevated fibrinogen and disturbed fibrinolytic activity may be related to the extent of disease within the femoro-popliteal arteries, more so than in the aorto-iliac arteries.

Adult↗

PubMed1996

High purity factor IX and prothrombin complex concentrate (PCC): pharmacokinetics and evidence that factor IXa is the thrombogenic trigger in PCC.

Recent studies using assays for surrogate markers of thrombogenicity in man have demonstrated that activation of the coagulation system occurs following infusion of clinical doses of prothrombin complex concentrates (PCC) but not after the same doses of high-purity factor IX concentrates (HP-FIX) in patients with haemophilia B. Here we have investigated the mechanism of such thrombogenesis by applying assays that detect early-through to late-events in coagulation system activation in a pharmacokinetic cross-over study of 50 IU/kg PCC and a new HP-FIX product in haemophilia B patients. Satisfactory recoveries and half-lives were observed for both concentrates. HP-FIX caused no increases in thrombin-antithrombin III complex (TAT), prothrombin activation peptide fragment F1+2 (F1+2), factor X activation peptide (FXAP) or factor VIIa (FVIIa). In contrast the same dose of factor IX in the form of PCC was followed by significant increases over pre-infusion levels of TAT, F1+2 and FXAP, but not FVIIa. Elevations of FIXAP occurred after both HP-FIX and PCC but did not reach normal levels and were attributed to normalisation of the FIX concentration in those patients whose levels of FIXAP were initially low. We conclude that the thrombogenic trigger associated with PCC infusion occurs at the level of factor X activation. In the absence of any increase in FVIIa, we would attribute this to the likely presence of FIXa in the PCC.

Adult↗

PubMed1995

Effects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms.

Cardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associations of left ventricular (LV) aneurysm formation and dysfunction with plasma fibrinogen, von Willebrand factor, and fibrin D-dimer, which are markers associated with thrombus formation (thrombogenesis) and to investigate the effects of warfarin given to patients with LV aneurysms on fibrinogen and D-dimer levels. A cross-sectional study of 112 patients with coronary artery disease was initially performed: 34 patients had normal LV function (group 1); 30 had LV dysfunction without aneurysm formation (group 2); 29 had LV aneurysms without anticoagulation (group 3a); and 19 patients had LV aneurysms with warfarin therapy (group 3b). Results were compared with 158 population controls from a random population sample. A longitudinal study of 10 patients given warfarin was also performed. In group 1, plasma fibrinogen (median difference 0.36 g/L; p = 0.0009) and von Willebrand factor (median difference 17 IU/dl; p = 0.04) were elevated, whereas plasma D-dimer levels (median difference 23.0 ng/ml; p = 0.001) were lower than those in population control subjects. There were no significant differences in plasma fibrinogen, von Willebrand factor, or D-dimer levels between groups 1 and 2. In group 3a, plasma fibrinogen was elevated when compared with group 1 (median difference 0.6 g/L; p = 0.0001), with a trend toward high von Willebrand factor levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1995

Is diastolic dysfunction associated with thrombogenesis? A study of circulating markers of a prothrombotic state in patients with coronary artery disease.

Clinical data on the contributory role of heart failure to thromboembolic risk does not differentiate between systolic and diastolic left ventricular dysfunction. We therefore conducted a population-controlled cross-sectional study to determine levels of plasma fibrinogen (associated with thromboembolism), fibrin D-dimer (a marker of fibrin turnover) and von Willebrand factor (a marker of endothelial dysfunction) in patients with ischaemic heart disease (a common cause of diastolic dysfunction) in whom left ventricular diastolic function was defined by echocardiography. We studied 106 patients: those with normal left ventricular function (n = 42, Group 1); those with left ventricular dysfunction but without aneurysms (n = 34, Group 2); and those with left ventricular aneurysm formation (n = 30, Group 3). Each of these groups was subdivided into those with (a) and without (b) diastolic dysfunction. Diastolic dysfunction was present in over 60% of patients, irrespective of left ventricular systolic impairment. There were no significant differences in median levels of plasma fibrinogen, fibrin D-dimer or von Willebrand factor in each group of patients with ischaemic heart disease, whether or not left ventricular diastolic dysfunction was present (Mann-Whitney test; P = N.S.). Systolic (rather than diastolic) dysfunction was the main correlate of these (analysis of variance, general linear model--ANOVA-GLM--P < 0.05) and the greatest abnormalities of fibrinogen, endothelial dysfunction and intravascular fibrin turnover were seen in patients with left ventricular aneurysms whether or not diastolic dysfunction was present. This study demonstrates that there is no evidence of a significant additional contribution to thrombotic risk (as assessed by plasma fibrinogen, von Willebrand factor and fibrin D-dimer) for patients with left ventricular diastolic dysfunction. A relationship is noted between some prothrombotic factors and Doppler indices of flow, which suggests a possible association between cardiac haemodynamics and thrombogenesis.

Analysis of Variance↗

PubMed1995

Tissue-plasminogen activator, plasminogen activator inhibitor and risk of peripheral arterial disease.

In this population-based case-control study, we examined the relationship between the fibrinolytic variables tissue-plasminogen activator (t-PA) antigen and plasminogen activator inhibitor (PAI) activity, cardiovascular risk factors and peripheral arterial disease. Cases and controls were selected from the Edinburgh Artery Study, a random sample survey of men and women, aged 55-74 years. Mean levels of t-PA antigen and PAI activity were significantly elevated in 121 cases compared to 126 controls. The increased risks of peripheral arterial disease with increasing PAI activity and t-PA antigen levels were partly mediated by interactions with serum triglycerides, high density lipoprotein (HDL) cholesterol and cigarette smoking. For example, adjustment for triglycerides significantly reduced the odds of disease for PAI activity from 1.41 (95% confidence intervals 1.08, 1.86) to 1.24 (0.93, 1.65) and from 1.47 (1.09, 1.98) to 1.34 (0.99, 1.82) for t-PA antigen. We conclude that impaired fibrinolytic potential (raised PAI activity and t-PA antigen) is associated with peripheral atherosclerosis and that this relationship is partly influenced by lipids and cigarette smoking.

Age Factors↗

PubMed1995

Plasma fibrinogen and fibrin D-dimer in patients with atrial fibrillation: effects of cardioversion to sinus rhythm.

Cardioversion of atrial fibrillation carries a serious risk of major thromboembolism and stroke. To determine whether or not the procedure alters plasma levels of fibrin D-dimer (a marker of intravascular fibrin turnover and thrombus formation) and plasma fibrinogen (associated with stroke and thromboembolism), we performed a prospective study in 19 patients with atrial fibrillation in whom cardioversion was attempted: seven patients without prior oral anticoagulant therapy (but with intravenous heparin for 24 h) (Group I), and 12 patients with full oral anticoagulation pre- and post-cardioversion (Group II). Plasma fibrinogen and fibrin D-dimer were measured pre-cardioversion, and at Days 3, 7 and 14 post-cardioversion. In Group I, there was a significant reduction in median plasma fibrin D-dimer levels by 14 days following cardioversion (200 vs. 52 ng/ml; paired Wilcoxon test, P = 0.02). In Group II, there was no change in median plasma fibrin D-dimer levels over the 14 days following cardioversion. There were no significant changes in plasma fibrinogen with cardioversion in either group of patients. The reduction of plasma fibrin D-dimer in Group I suggests a beneficial reduction of intravascular fibrin turnover and thrombogenesis by the cardioversion of patients with atrial fibrillation to sinus rhythm. Furthermore, it strongly suggests that it is atrial fibrillation itself which is the major risk of thromboembolism and that the risk continues for up to 14 days post-cardioversion. In Group II, the low pre-cardioversion fibrin D-dimer levels and lack of change with cardioversion is consistent with the prophylactic effect of warfarin therapy against thromboembolism during the cardioversion of atrial fibrillation.

Adult↗

PubMed1995

Fibrinogen and markers of fibrinolysis and endothelial damage following resolution of critical limb ischaemia.

OBJECTIVES: To assess the effects of resolution of critical limb ischaemia on the elevated plasma fibrinogen, cross-linked fibrin degradation products (FDP), and von Willebrand factor antigen (vWF) levels, reported in peripheral arterial occlusive disease. DESIGN: A prospective study of patients undergoing surgery for chronic critical limb ischaemia. SETTING: Two vascular surgery units providing tertiary referral services for the West of Scotland. MATERIALS: Venous blood samples were assayed for plasma fibrinogen, FDP D-dimer, and vWF levels, prior to surgery, together with fibrinolytic and rheological parameters, in 82 patients. Sampling was repeated 4 months after resolution of critical limb ischaemia. OUTCOME MEASURES: Levels of these parameters following successful resolution of critical limb ischaemia were compared with pre-operative levels, and with an age-matched random population sample. MAIN RESULTS: Plasma fibrinogen and vWF levels were significantly lower (both p < 0.005, Wilcoxon matched pairs) following successful resolution of critical limb ischaemia in the 56 patients available for review, although levels remained higher than in population controls (p < 0.01, Mann-Whitney U-test). FDP levels were unchanged following surgery, remaining higher than in age-matched population controls (p < 0.01). CONCLUSIONS: Resolution of critical limb ischaemia fails to reduce plasma fibrinogen, fibrin turnover, and vWF levels to those seen in population controls. This implies that increased fibrinogen and fibrin turnover in peripheral arterial disease is not solely a consequence of tissue ischaemia, while the persisting prothrombotic state following resolution of critical limb ischaemia has potentially important implications for graft and patient survival.

Aged↗

PubMed1995

Increased markers of thrombogenesis in chronic atrial fibrillation: effects of warfarin treatment.

OBJECTIVE: To determine whether chronic atrial fibrillation is associated with abnormalities in plasma fibrinogen, von Willebrand factor (vWF) (a marker of endothelial disturbance), or fibrin D- dimer (a measure of fibrin turnover); and if so, whether such levels are related to haemodynamic disturbance (enlarged left atrium, poor left ventricular function) or existing treatment with warfarin or aspirin. To investigate the effects of introducing warfarin in patients with atrial fibrillation on fibrinogen and D- dimer levels. DESIGN: Cross sectional population sample controlled study and longitudinal study of patients undergoing anticoagulation. SETTING: District general hospital. SUBJECTS: 87 patients (44 men and 43 women of mean (SEM) age 63.0 (1.0)) with chronic atrial fibrillation. At the time of the study, 37 were taking no antithrombotic medication (group 1), 31 were taking warfarin (including two on warfarin and aspirin) (group 2) and 19 were taking aspirin alone (group 3). They were compared with 158 population controls from a random population sample (the second Glasgow monitoring trends and determinants in cardiovascular disease study). As part of clinical treatment warfarin was introduced in 20 patients with chronic atrial fibrillation (14 men and six women of mean (SEM) (range) age 63.9 (2.35 (32-74) years). RESULTS: Plasma fibrinogen remained significantly increased in patients of group 1 (no antithrombotic medication) compared with that of the population controls (median difference 1.23 g/l; 95% confidence interval (CI) 0.88 to 1.62, P < 0.0001). There was also a significant increase in plasma D-dimer levels (median difference 77 ng/ml; 95% CI 38 to 122, P < 0.01) and vWF (median difference 63 IU/dl; 95% CI 38 to 89, P < 0.0001). There was no significant difference in plasma fibrinogen (median difference 0.14 g/l; 95% CI -0.44 to 0.77, P = 0.65) or vWF (median difference 3.5 IU/dl; 95% CI - 41 to 41, P = not significant in patients of group 2 (warfarin treatment) compared with that of patients in group 1. Levels of D-dimer were significantly lower in group 2 (median difference 90 ng/ml, 95% CI 39 to 150, P < 0.0001) than in group 1. There were no significant differences in plasma fibrinogen (median difference 0.08 g/l; 95% CI - 0.52 to 0.77, P = 0.73), D-dimer (median difference - 34 ng/ml; 95% CI - 114 to 21.0, P = 0.25), or vWF (median difference 2%; 95% CI - 35 to 41, P = not significant) levels between patients of groups 1 and 3. There were no significant correlations between the coagulation indices and left atrial volume or ventricular function. There was a significant positive correlation between plasma fibrin D-dimer and vWF levels in patients of groups 1 and 3 (r = 0.52, P < 0.001). There was a significant reduction in median plasma fibrin D-dimer levels at 2 months after the introduction of warfarin (181 ng/ml v 80 ng/ml, P < 0.001), but no effect on plasma fibrinogen. CONCLUSIONS: Increased median plasma fibrinogen and vWF levels were found in patients with chronic atrial fibrillation. Plasma D-dimer levels were also increased in patients with chronic atrial fibrillation not receiving warfarin, suggesting increased intravascular thrombogenesis in such patients. Introduction of warfarin normalised circulating fibrin D- dimer levels, suggesting that warfarin treatment was effective in preventing excessive fibrin turnover, consistent with the antithrombotic effects of warfarin. These results suggest three possible thrombotic markers to assess patients with atrial fibrillation who are at high risk of thrombogenesis; D-dimer also merits assessment as a measure of reduction in thrombotic risk in patients receiving warfarin.

Adult↗

PubMed1995

Determinants of fibrin D-dimer in the Edinburgh Artery Study.

There is growing evidence that fibrin D-dimer is associated with coronary and peripheral atherosclerosis. Using data from the Edinburgh Artery Study, we examined the distribution of fibrin D-dimer in 1592 men and women 55 to 74 years old and assessed its relationship with a range of cardiovascular risk factors. Fibrin D-dimer levels were higher in women than in men (P < or = .05) and increased with age (P < or = .001). Current cigarette smokers had higher levels than ex-smokers, who, in turn, had higher levels than those who had never smoked. On multiple regression analyses with age and plasma fibrinogen as covariates, only lifetime smoking in men and systolic blood pressure in women were independent predictors of fibrin D-dimer levels. Since fibrin D-dimer does not appear to be independently related to many of the common cardiovascular risk factors, it may be a useful index of the thrombotic contribution to arterial disease.

Aged↗

PubMed1995

Fibrin D-dimer, haemostatic factors and peripheral arterial disease.

Several haemostatic factors have been shown to have a predictive role in cardiovascular disease, although their relationship with prevalent peripheral arterial disease is not well reported. Using a random sample of 1592 men and women aged 55-74 years from Edinburgh, Scotland, we examined the relationship of von Willebrand factor (vWF), tissue plasminogen activator (t-PA) and fibrin D-dimer antigens and factor VII activity to peripheral arterial disease. t-PA antigen and fibrin D-dimer showed significant linear trends of increased levels with increasing severity of disease in both sexes (p < or = 0.01) and vWF showed a similar pattern in men only (p < or = 0.01). On multivariate analysis, fibrin D-dimer was independently related to the risk of intermittent claudication (p < or = 0.01) and, among men, to the extent of arterial narrowing in the lower limb, as measured by the ankle brachial pressure index, (ABPI) (p < or = 0.001). These results are further evidence of a role for intravascular fibrin deposition in the development of peripheral atherosclerosis.

Aged↗

PubMed1995

Relation of haemostatic, fibrinolytic, and rheological variables to the angiographic extent of peripheral arterial occlusive disease.

We investigated the relationships between the angiographic severity of peripheral arterial occlusive disease (PAOD) and haemostasis, fibrinolytic, and rheological variables in 219 patients with symptomatic peripheral arterial occlusive disease (PAOD). White cell count, fibrinogen, cross-linked fibrin degradation products (FDP), von Willebrand factor, and plasminogen activator inhibitor levels were all elevated in comparison with age-matched population controls (all p < 0.0001, Mann-Whitney U test), while fibrinogen (Spearman r = 0.30), von Willebrand factor (r = 0.40), and log (FDP) (r = 0.56), (all p < 0.0001) showed a strong correlation with the angiographic extent of PAOD. Multivariate analysis indicated that log (FDP) was a strong independent predictor of the angiographic severity of PAOD (p < 0.0001), in addition to increasing age (p < 0.0001), presence of tissue sepsis (p < 0.02), prior vascular surgery (p = 0.007), and other vascular pathology (p = 0.007). These results confirm that increase in fibrinogen, von Willebrand factor, plasminogen activator inhibitor and fibrin turnover, are strongly associated with the presence of symptomatic peripheral arterial disease, and suggest that there may be a causal link between fibrin turnover, as determined by FDP levels, and the extent of peripheral arterial occlusive disease.

Adult↗

PubMed1995

Relation of haemostatic, fibrinolytic, and rheological variables to the angiographic extent of peripheral arterial occlusive disease.

We investigated the relationships between the angiographic severity of peripheral arterial occlusive disease (PAOD) and haemostasis, fibrinolytic, and rheological variables in 219 patients with symptomatic peripheral arterial occlusive disease (PAOD). White cell count, fibrinogen, cross-linked fibrin degradation products (FDP), von Willebrand factor, and plasminogen activator inhibitor levels were all elevated in comparison with age-matched population controls (all p < 0.0001, Mann-Whitney U test), while fibrinogen (Spearman r = 0.30), von Willebrand factor (r = 0.40), and log (FDP) (r = 0.56), (all p < 0.0001) showed a strong correlation with the angiographic extent of PAOD. Multivariate analysis indicated that log (FDP) was a strong independent predictor of the angiographic severity of PAOD (p < 0.0001), in addition to increasing age (p < 0.0001), presence of tissue sepsis (p < 0.02), prior vascular surgery (p = 0.007), and other vascular pathology (p = 0.007). These results confirm that increases in fibrinogen, von Willebrand factor, plasminogen activator inhibitor and fibrin turnover, are strongly associated with the presence of symptomatic peripheral arterial disease, and suggest that there may be causal link between fibrin turnover, as determined by FDP levels, and the extent of peripheral arterial occlusive disease.

Age Factors↗